Advances on pathogenesis research of acute myeloid leukemia with t(8;21)-- review / 中国实验血液学杂志
Journal of Experimental Hematology
; (6): 1632-1637, 2010.
Article
in Zh
| WPRIM
| ID: wpr-332303
Responsible library:
WPRO
ABSTRACT
Acquired chromosomal translocations can be identified in nearly 50% of human acute myeloid leukemias. The common chromosomal translocation in this disease is t(8;21) (q22;q22). It involves the aml1 (runx1) gene on chromosome 21 and the eto (mtg8, runx1t1) gene on chromosome 8 generating the aml1/eto fusion gene. An initial model for its pathogenesis emphasized the conversion of a hematopoietic transcriptional activator AML1 into a leukemogenic repressor which blocked myeloid differentiation at the level of target gene regulation. Aml1/eto fusion genes inhibit key hematopoietic transcription factor that function as tumor suppressors at several nodal point during hematopoietic differentiation. A new model is presented in which aml1/eto coordinates expansion of the stem cell compartment with diminished lineage commitment and with genome instability. In this review, the molecular role of aml1/eto fusion gene and his transcribed isoforms in regulating stem renewal, blocking hematopoietic differentiation and interacting with various lineage-specific transcription factors are summarized.
Full text:
1
Index:
WPRIM
Main subject:
Pathology
/
Chromosomes, Human, Pair 8
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Chromosomes, Human, Pair 21
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Leukemia, Myeloid, Acute
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Oncogene Proteins, Fusion
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Core Binding Factor Alpha 2 Subunit
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RUNX1 Translocation Partner 1 Protein
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Genetics
Type of study:
Etiology_studies
/
Prognostic_studies
Limits:
Humans
Language:
Zh
Journal:
Journal of Experimental Hematology
Year:
2010
Type:
Article